Biomedical subjects

M Sabetkasai

Publications and source records attributed to M Sabetkasai.

7 recordsLinked to original sources

PubMed1999

Baclofen and antidepressant--induced antinociception in formalin test: possible GABA(B) mechanism involvement.

In this study, the influences of GABA(B) agents on antidepressant-induced antinociception in the mouse formalin test have been investigated. The GABA(B) receptor agonist baclofen (2.5, 5 and 10 mg/kg) induced a dose-dependent antinociception in the second phase of the formalin test. This response was inhibited by the GABA(B) receptor antagonist, CGP35348 [P-(3-aminopropyl)-p-diethoxymethyl-phosphinic acid], in a dose-dependent manner. The antagonist by itself also induced antinociception. Single administration of the antidepressants citalopram (10, 20, 40 and 80 mg/kg), desipramine (20, 40, 80 mg/kg) or imipramine (10, 20 and 40 mg/kg) also induced antinociception in both phases of the formalin test. CGP35348 (100 and 200 mg/kg) pretreatment reduced the response induced by the tricyclic antidepressants. A combination of baclofen with the tricyclic antidepressant did not potentiate antinociception induced by antidepressants, but a decrease in the response induced by higher dose of baclofen was shown. It is concluded that GABA mechanism(s) may modulate the antidepressant-induced antinociception.

Analgesics, Non-Narcotic↗

PubMed1999

Baclofen-induced antinociception and nicotinic receptor mechanism(s).

In this study, the influences of nicotinic receptor agents on baclofen-induced antinociception in the tail-flick test have been studied. Intraperitoneal administration of baclofen (2.5, 5 and 10 mg/kg) to mice induced a dose-dependent antinociception in the tail-flick test. Subcutaneous injection of nicotine (0.5-2.5 mg/kg) also caused a dose-dependent antinociceptive response. Intracerebral (10 and 20 microg/mouse) but not intraperitoneal administration of hexamethonium (5 and 10 mg/kg) to mice decreased the response of both nicotine and baclofen. However, administration of the GABA(B) antagonist CGP 35348 (100 and 200 mg/kg) decreased the response induced by baclofen but not by nicotine. It is concluded that at least part of the baclofen-induced antinociception may be mediated through a nicotinic mechanism.

Analgesics↗

PubMed1997

Opposite influences of different adrenoceptors on baclofen-induced antinociception in mice.

In the present study, the effects of adrenoceptor agonists and antagonists on baclofen-induced antinociception was investigated. Intraperitoneal administration of different doses of baclofen (2.5, 5 and 10 mg/kg) induced antinociception in the tail-flick test. The response was dose-dependent. The alpha 2-adrenoceptor agonist, clonidine, increased, while the alpha 1-adrenoceptor agonist, phenylephrine, decreased the baclofen response. In reserpine-treated animals, alpha 2-adrenoceptor, clonidine, induced antinociception and increased that of baclofen. Yohambine and propranolol but not prazosin decreased the baclofen effect. Although phenoxybenzamine itself induced antinociception it did not alter the baclofen response significantly. Reserpine treatment decreased the response induced by single administration of baclofen or phenoxybenzamine and that induced by a combination of baclofen with either phenoxybenzamine or prazosin. It may be concluded that alpha 2-adrenoceptor stimulation increases, while alpha 1-adrenoceptor activation decreases the baclofen-induced antinociception, and aminergic mechanism(s) may have a positive influence on baclofen response.

Adrenergic Agonists↗

PubMed1993

Influences of different adenosine receptor subtypes on catalepsy in mice.

The effects of adenosine A1 and A2 receptors on catalepsy were studied in mice. The adenosine agonists 5-N'-ethylcarboxamide-adenosine (NECA), N6-phenylisopropyladenosine (PIA) and N6-cyclohexyladenosine (CHA) induced dose dependent catalepsy. The A1 adenosine antagonist 8-phenyltheophylline (8-PT) potentiated catalepsy induced by NECA, R-PIA and CHA. However, theophylline did not potentiate but inhibited the responses induced by NECA, R-PIA and CHA. Neither 8-PT nor theophylline alone has any effect on catalepsy in mice. It is concluded that catalepsy induced by the adenosine agonists may be due to A2 receptor stimulation and that the A1 antagonism may potentiate the response.

Adenosine↗

PubMedDate not supplied

Stress-induced antinociception and GABAergic mechanism.

The antinociceptive effects of GABAergic agents in presence or absence of swim-stress were investigated in mice, using the tail-flick test. Swim-stress, the GABAB agonist baclofen and the GABAA agonist muscimol raised the threshold of withdrawal reactions to nociceptive stimulation. The antinociception, induced by an interaction of stress and GABA agonists, was higher than that of stress or a GABA agonist alone. The GABAB antagonist phaclofen and the GABAA antagonists bicuculline and picrotoxin decreased the antinociceptive action induced by stress plus baclofen. Picrotoxin administration also decreased the response of baclofen. Picrotoxin and biculline, but not phaclofen, reduced the antinociceptive response induced by muscimol in stressed mice. Administration of picrotoxin, bicuculline or phaclofen alone did not decrease the stress-induced antinociception. The antagonists even increased the base line latencies in both normal and stressed mice. It is concluded that stimulation of both GABAA and GABAB receptor sites has an antinociceptive effect, but that the involvement of a GABAergic mechanism in stress-induced antinociception is unlikely.

Analgesics↗

PubMedDate not supplied

Effects of drugs active at adenosine receptors on stress-induced analgesia in mice.

Mice were stressed by swimming for 3 min in water at 20 degrees C and antinociception was assessed by the tail-flick test. The stress-induced antinociception was potentiated by intraperitoneal administration of different doses of theophylline. The effect of the drug was dose-dependent. 5'-N-Ethylcarboxamidoadenosine administration also increased the stress response dose-dependently. N6-Phenyl-isopropyladenosine decreased the antinociception induced by swim-stress as well as after stress plus theophylline. Administration of dipyridamole caused a decrease of antinociception induced by stress or stress plus theophylline. It may be concluded that activation of A2 adenosine receptors increased whereas activation of A1 adenosine sites decreased the stress-induced antinociception. The responses of A2 or A1 activation may be irrelevant to changes in cAMP levels. Because the adenosine agonists and antagonists employed were not selective at the receptor level, other possibilities are not excluded.

Adenosine↗

PubMedDate not supplied

Antinociception: interaction between adenosine and GABA systems.

The interaction of GABA agonists and antagonists with the antinociceptive effects of drugs active on adenosine receptors, was examined in mice using the tail-flick test. Baclofen, but not muscimol (in the doses used), induced antinociception. The adenosine agonist NECA (5'-N-ethylcarboxamidoadenosine) produced a greater degree of antinociception than did PIA (N6-phenylisopropyladenosine). The antinociceptive effect of NECA and PIA was decreased by the GABA antagonists bicuculline, picrotoxin and phaclophen. Combination of theophylline with baclofen, but not with muscimol, induced a high antinociceptive response. Muscimol decreased the antinociceptive effect of NECA, and baclofen increased the antinociceptive action of PIA. It is concluded that there may be an interaction between antinociception induced by GABA and that induced by (an) adenosine mechanism(s).

Adenosine↗